Korewicki J, Rajecka A, Pogorzelska H, Madeja G
Kliniki Wad Serca Instytutu Kardiologii.
Kardiol Pol. 1990;33(6):365-74.
During exercise in subjects with congestive heart failure and mitral regurgitation the rise in systemic arterial pressure is usually accompanied by increase in systemic vascular resistance. That could cause decrease of cardiac output not only because of a lack of myocardial reserve, but also because of an increase of mitral regurgitant volume. In such situation decrease in left ventricular preload could further increase the regurgitant volume and cardiac output. Whether changes in pre-or afterload can cause significant changes in mitral regurgitation, nitroglycerin and phentolamine was assessed in that group of patients. 22 patients with significant mitral regurgitation (3+,4+) was randomly divided into two groups. The first one received short intravenous infusion of nitroglycerin at a rate of 170 micrograms/min. The second one received phentolamine intravenously 1-1,5 mg/min. Patients underwent right heart catheterization with Swan-Ganz thermodilution catheter. Mean pulmonary, pulmonary capillary wedge, and right atrial pressure were monitored and recorded. Cardiac output was determined by thermodilution technique using iced 5% dextrose. If there were no contraindications (PWP greater than 30 mm Hg) an effort test was performed (cycloergometer, supine position). The same protocol was repeated during administration of nitroglycerin and phentolamine. Nitroglycerin significantly decreased right atrial and capillary wedge pressure (from 22.9 to 15.6 mm Hg). There were no significant differences in cardiac output, pulmonary and systemic vascular resistance. Pulmonary artery pressure decreased after nitroglycerin but the difference was not significant. All above effects of nitroglycerin persisted during effort. Phentolamine decreased significantly right atrial, pulmonary and capillary wedge pressure with simultaneous increase of cardiac output (30%) and decrease of pulmonary and systemic vascular resistance. In summary, nitroglycerin decreases only symptoms and theoretically could worsen forward flow in patients with mitral regurgitation and heart failure, especially in subjects with a significant increase of systemic vascular resistance during effort.
在充血性心力衰竭和二尖瓣反流患者运动期间，体循环动脉压升高通常伴随着体循环血管阻力增加。这不仅会因心肌储备不足导致心输出量减少，还会因二尖瓣反流容积增加而减少心输出量。在这种情况下，左心室前负荷降低会进一步增加反流容积和心输出量。为评估前负荷或后负荷变化是否会导致二尖瓣反流发生显著变化，对该组患者使用了硝酸甘油和酚妥拉明。22例重度二尖瓣反流（3 +、4 +）患者被随机分为两组。第一组以170微克/分钟的速率静脉输注短效硝酸甘油。第二组静脉注射酚妥拉明，速度为1 - 1.5毫克/分钟。患者使用Swan - Ganz热稀释导管进行右心导管检查。监测并记录平均肺动脉压、肺毛细血管楔压和右心房压力。使用冰5%葡萄糖通过热稀释技术测定心输出量。如果没有禁忌证（肺毛细血管楔压大于30毫米汞柱），则进行负荷试验（卧式测力计，仰卧位）。在给予硝酸甘油和酚妥拉明期间重复相同方案。硝酸甘油显著降低右心房和毛细血管楔压（从22.9降至15.6毫米汞柱）。心输出量、肺血管阻力和体循环血管阻力无显著差异。硝酸甘油使肺动脉压降低，但差异不显著。硝酸甘油的所有上述作用在负荷试验期间持续存在。酚妥拉明显著降低右心房、肺动脉和毛细血管楔压，同时心输出量增加（30%），肺血管阻力和体循环血管阻力降低。总之，硝酸甘油仅减轻症状，理论上可能会使二尖瓣反流和心力衰竭患者的前向血流恶化，尤其是在运动期间体循环血管阻力显著增加的患者中。
